A more recent study found that following cytarabine chemotherapy, the enriched-senescent AML cells produced a senescence-associated secretory phenotype (SASP) by increasing NF-κB transcription through the ataxia telangiectasia and Rad3-related (ATR) activities, and regained stemness properties sufficient to restore leukemia (129). The gene discussed is NFKB1; the disease is acute myeloid leukemia.